It is our impression that relatively early atherosclerotic lesions can be manipulated favorably by elevating endogenous PTH levels in the presence of low to normal serum calcium levels. We have used EDTA to effect this manipulation. We have to date not had an opportunity to investigate either aortic connective tissue metabolism per se or the odds of altering it in animals with atherosclerosis of long standing. One or two experiments to elucidate this are high on our list of priorities under the moneys requested herewith. An attempt will be made to distinguish between reversal and/or inhibition of the atherosclerotic process by the EDTA - PTH mechanism. We would like to verify that the proposed mechanism, i.e., EDTA injection complexes calcium which in turn stimulates the endogenous PTH production which is the immediate agent responsible for the observed effects, is the de facto mechanism. We wish to study the effect of PTH on vascular connective tissue in vivo. The objective will be to discover differences, if any, between the action of the hormone on growing as compared to adult animals; pathological as compared to normal tissue, and to elucidate the effects of the hormone on the synthetic versus the degradative aspects of the connective tissue metabolism. Finally we wish to relate the aortic mucopolysaccharide metabolism to that of tissue collagen and elastin in atherogenesis.